TY - JOUR
T1 - In This Issue of <em>Diabetes</em>
JF - Diabetes
JO - Diabetes
SP - 2465
LP - 2466
M3 - 10.2337/db16-ti09
VL - 65
IS - 9
A2 - ,
Y1 - 2016/09/01
UR - http://diabetes.diabetesjournals.org/content/archive/65/9/2465/1.abstract
N2 - By Max Bingham, PhDAn enzyme that normally breaks down the major extracellular matrix component hyaluronan may be the key to explaining various vascular complications in diabetes. In particular, it seems likely that hyaluronidase activity exacerbates endothelial dysfunction in diabetes. The study by Dogné et al. (p. 2742) focuses on HYAL1 knockout mice and control wild-type mice and examines the effect of HYAL1 on endothelial (dys)function markers in the presence or absence of streptozotocin-induced diabetes. Specifically they examined the effects of the deletion on endothelial markers, endothelial-dependent vasodilation, arteriolar glycocalyx size, and glomerular barrier function. According to the authors, the lack of HYAL1 conferred a number of beneficial effects in the mice when diabetes was also present. In terms of endothelial dysfunction, the lack of HYAL1 prevented increases in P-selectin (a cell adhesion molecule) while a measure of vasodilation suggested better protection in the knockout mice. Glycocalyx thickness and structure (as well as hyaluronan content) were also better preserved in the presence of diabetes in the knockout mice as compared to the wild-type mice. The lack of HYAL1 also completely prevented diabetes-induced glomerular barrier dysfunction (where the kidney’s ability to filter blood becomes impaired), further suggesting beneficial effects toward glycocalyx preservation. As for mechanisms, the authors suggest the absence of the HYAL1 enzyme prevents glycocalyx from shedding hyaluronan during diabetes and this in turn prevents a whole series of events leading ultimately to vascular damage and attendant (clinical) complications. Commenting more widely on the study, author Sophie Dogné said: “The expression of the hyaluronidase enzyme, HYAL1, is increased in all forms of diabetes, whether experimental or human diabetes. Our study suggests this increase is linked to early endothelium and glycocalyx damage. We intend …
ER -